An antibody raised against acyl-CoA:monoacylglycerol acyltransferase 1 1 (MGAT1); acylates monoacylglycerol to form diacylglycerol, a key building block of physiological lipids.
Catalogue number crb2005750 Antibody Anti-MGAT1 antibody Antigen Peptide KLH conjugated synthetic peptide crb1200959 Protein ID UniProtKB - Q96PD6 (Human) Aliases 2-acylglycerol O-acyltransferase 1, Acyl-CoA:monoacylglycerol acyltransferase 1 (MGAT1), Diacylglycerol O-acyltransferase candidate 2 (hDC2), Diacylglycerol acyltransferase 2-like protein 1, Monoacylglycerol O-acyltransferase 1 Cross-Reactivity Human Host Species Rabbit Antibody Type Polyclonal Concentration 2.0 mg/ml Glycine Target MGAT1 Family Diacylglycerol acyltransferase family Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References
Agarwal et al., (2016). Mogat1 deletion does not ameliorate hepatic steatosis in lipodystrophic (Agpat2−/−) or obese (ob/ob) mice. J. Lipid Res., 57(4): 616. doi: 10.1194/jlr.M065896.
Lutkewitte et al., (2021). Multiple antisense oligonucleotides targeted against monoacylglycerol acyltransferase 1 (Mogat1) improve glucose metabolism independently of Mogat1. Mol. Metab., 49: 101204. doi: 10.1016/j.molmet.2021.101204.
Acyl-CoA:monoacylglycerol acyltransferase 1 (MGAT1) acylates monoacylglycerol to form diacylglycerol. MGAT activity is part of the MGAT pathway which allows the storage of neutral triacylglycerol (TAG). This is an auxillary pathway to the glycerol-3-phosphate (G-3-P) pathway. MGAT1 is highly expressed in adipocytes and may function to suppress aberrant lipolysis, which can lead to steatosis. MGAT isoforms (MGAT1, MGAT2, MGAT3) are increased in humans and mouse models of nonalcoholic fatty liver disease (NAFLD). Antisense oligonucleotides (ASO) have been used to reduce hepatic MGAT activity, which was independent of MGAT1. This improves hepatic insulin sensitivity and glucose metabolism without affecting hepatic DAG or TAG levels in obese mice models. The TAG synthesis in steatosis associated with lipodystrophy and obesity minimally depends on MOGAT1. The study of MGAT1 aims to improve understanding of insulin resistance and steatosis and better elucidate the function of MGAT1 compared to MGAT2 and MGAT3.